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目的 :探讨氯化甲基汞中毒大鼠周围神经损伤的病理改变及病理机制。 方法 :在 WKAH大鼠服用氯化甲基汞 4mg/ d所致的亚急性汞中毒模型上 ,采用组织病理、免疫组化、蛋白印迹等方法动态观察坐骨神经和后根神经节的病理演变 ,TU NEL 染色观察细胞凋亡。 结果 :中毒后第 11天后根神经节内可见散在大型神经元 A被吞噬细胞浸润 ,电镜下 A型神经元胞质内线粒体变性 ;坐骨神经远端轻微轴索变性 ,病变逐渐加重并向心性发展。第 15天开始出现髓鞘崩解 ,MRF- 1染色显示有少量的吞噬细胞反应。第 18天出现明显轴索变性及髓鞘崩解 ,可见大量浸润的吞噬细胞 ;后根神经节内 A型神经元近于消失 ,但 B型神经元保留良好 ,B型神经元的上行终末胶状质下区亦出现明显变性。TUNEL 染色未观察到节细胞凋亡。采用Western印迹法观察到坐骨神经及后根神经节神经原纤维及髓鞘蛋白 O随中毒时间延长逐渐降低 ,在第 15天后尤为明显 ,与免疫组化结果相符合。结论 :亚急性汞中毒模型中 ,A型神经元变性可能与汞中毒损伤线粒体膜继发的能量代谢障碍有关 ;而B型神经元变性则符合逆行性死亡的过程。
Objective: To investigate the pathological changes and pathological changes of peripheral nerve injury induced by methylmercury chloride in rats. Methods: Pathological changes of the sciatic nerve and the dorsal root ganglion were observed dynamically by histopathology, immunohistochemistry and Western blot in a model of subacute mercury poisoning induced by MeHg 4 mg / d in WKAH rats. TU NEL staining observed apoptosis. Results: A large neuron A was infiltrated by phagocytes in the root ganglion 11 days after poisoning. Mitochondrial degeneration was observed in the cytoplasm of type A neurons by electron microscopy. A slight axonal degeneration was found in the distal part of sciatic nerve. The lesion gradually aggravated and developed toward the heart. Myelin disintegration started on day 15, and MRF-1 staining showed a small amount of phagocytic reaction. A significant axonal degeneration and disintegration of myelin appeared on the 18th day. A large number of infiltrating phagocytes were seen. Type A neurons in the dorsal root ganglion almost disappeared, but the type B neurons remained well. The type B neurons’ Gel area also showed obvious degeneration. TUNEL staining showed no apoptotic cell death. The expression of neurofibrillar and myelin protein O in sciatic nerve and dorsal root ganglion neurons decreased gradually with the prolongation of poisoning time by Western blotting, especially after 15 days, which was in accordance with the immunohistochemical results. Conclusion: In the model of sub-acute mercury poisoning, the degeneration of type A neurons may be related to the energy metabolism disorder secondary to mitochondrial membrane damage caused by mercury poisoning. The degeneration of type B neurons is in line with the process of retrograde death.